Immunoregulatory T cells, LFA-3 and HLA-DR in autoimmune thyroid diseases

Abstract

Aim:The aim of the present study was to examine the changes in the expression of T-cell activation markers, namely CD4+ CD25+ and CD8+ in patients with AITD, namely Graves’ disease and Hashimoto's thyroiditis as well as colloid nodular goitre. HLA-DR, LFA-3, and peripheral total lymphocytic count are also measured.Materials and Methods:We compared the expression of CD4, CD25, and CD8 surface markers in peripheral blood lymphocyte in Graves’ disease and Hashimoto's thyroiditis as autoimmune thyroid diseases, as well as colloid goitre in comparison with healthy controls. Also, LFA-3 and HLA-DR were measured in the same groups using three-color flow cytometry. Total lymphocytic count in peripheral blood, thyroid function tests, antithyroid antibodies were also included in the laboratory investigations. The total number of participants was 65. All were recruited from endocrine clinics in a tertiary care hospital in the southern region of Saudi Arabia. All participants underwent history taking, clinical examination, laboratory workup, and radiological investigations. Neck ultrasound, technecium pertechnetateψψ thyroid uptake, and fine-needle aspiration and cytology (FNAC) of the thyroid were done when indicated. The study was approved by the Hospital Research Isthics Committee and informed consents were obtained from all participants before enrollment in the study.Results:In comparison with thecontrol group, activation markers CD4, CD25, and CD8 were lower in the autoimmune thyroid diseases. Lymphocyte function antigen-3 (CD58) and total lymphocytic count were higher in the AIT diseases whereas HLA-DR was lower than that in the control group. The CD4/CD8 ratio was lower in the AITD compared with the healthy euthyroid subjects. No difference was found between patients with colloid nodular goitre and the healthy control in any of the study variables except for LFA-3 which was significantly higher in the colloid goitre group.Conclusion:Our findings indicate downregulation of CD4+ CD25+ Treg as well as CD8+ T cells in autoimmune thyroid diseases. Downregulation of suppressor T lymphocytes helps initiation, progression, and maintenance of the autoimmune thyroid diseases. Lower HLA-DR and higher CD58 in AITDs indicate their role in the expression of the autoantigen and its escape from the immune surveillance. High levels of LFA-3 in colloid goitre indicate that the autoimmune process needs interacting factors, and not only the high level of LFA-3.

Association of CD117 and HLA‑DR expression with shorter overall survival and/or progression‑free survival in patients with multiple myeloma treated with bortezomib and thalidomide combination treatment without transplantation

“…The HLA-DR antigen, which is encoded by the HLA-II gene, most frequently appears on the cytomembrane of macrophages and B lymphocytes and may aid the host immune system to identify and attack tumor cell ( 28 ). Previously, research regarding HLA-DR concentrated on diseases associated with the immune system ( 29 , 30 ) and solid tumors. Diao et al ( 31 ) indicated that overexpression of HLA-DR is associated with decreased OS in patients with glioma, while Sconocchia et al ( 32 ) reported that HLA class II antigen served as a favorable prognostic marker in patients with colorectal carcinoma.…”

Dysregulated Antibody, Natural Killer Cell and Immune Mediator Profiles in Autoimmune Thyroid Diseases

“…Pathologically, AITD are characterized by autoantibodies against three main thyroid proteins (thyroid peroxidase (TPO), thyroglobulin (Tg), and the thyroid-stimulating hormone (TSH) receptor (TSH-R)), infiltration of the thyroid gland by immune cells (e.g., lymphocytes, NK cells, monocytes, and macrophages), the formation of germinal centers in the thyroid gland [8] and dysregulated TSH levels [9,10]. However, some studies have failed to observe a significant difference in peripheral blood immune cell composition between AITD patients and healthy individuals [11], while others report significant differences in particular cell types or in immune marker expression [12]. Immune cells, thyroid autoantibodies, and secreted proteins including cytokines may play critical roles in AITD development [13] and in immune responses, including in antibody-dependent cell-mediated cytotoxicity (ADCC) pathways [14,15].…”

Multi-omic analyses reveal antibody-dependent natural killer cell-mediated cytotoxicity in autoimmune thyroid diseases

“…Some studies have failed to observe a significant difference in peripheral blood immune cell composition between AITD patients and healthy individuals 15 , whereas others have reported significant differences in particular cell types or specific marker expression on immune cells. 16 . Immune cells, thyroid autoantibodies, and secreted proteins including cytokines may play critical roles in AITD development 17 and could participate in immune responses including antibody-dependent cell-mediated cytotoxicity (ADCC) pathways 18, 19 .…”